Life-threatening pulmonary toxicity as a result of anticancer drug therapy is becoming increasingly recognized. It is also becoming apparent that because of the inherent molecular properties of some antineoplastic agents, reactive oxygen may be involved in the cytotoxic reaction(s) to lung cells. The drug-induced generation of reactive forms of oxygen (superoxide anion, hydroxyl radical and singlet oxygen) can contribute to drug cytotoxicity through attack of reactive oxygen species on intracellular targets (nucleic acids, lipids, proteins) and/or through reactive oxygen-mediated activation of the drug to an active intermediate. The present projects were designed to evaluate these hypotheses in order to better understand the possible biochemical and molecular mechanisms which contribute to pulmonary toxicity elicited by antineoplastics.